Study shows how neural networks adapt to the presence of a toxic HIV protein.
The incidence of HIV-associated dementia has declined dramatically since the introduction of potent combined antiretroviral therapy; however, milder forms of HIV-associated neurocognitive disorders (HAND) persist. Some 30 to 50 % of HIV-infected individuals have HAND. With an increasing proportion of HIV-infected individuals at risk of HAND, the development of a treatment and mapping of pathology is critical. Now, a study from researchers at the University of Minnesota shows that the HIV protein transactivator of transcription (Tat) alters the activity of networked neurons and that the network adapted to the presence of the toxin. The team state that Tat alters the excitability of networked neurons by a process that requires binding to cell surface proteins, and the activity of the networked neurons adapted in the sustained presence of the HIV protein. The study is published in the journal Current HIV Research.
Previous studies show the HIV-1 transactivator of transcription (Tat) protein is released by infected cells and contributes to the pathogenesis of HAND, however, many of the underlying mechanisms remain poorly understood. Also, infection with HIV is associated with increased incidence of new-onset seizures in a significant percentage of patients, once again the specific cause of seizure disorders remains unknown. The current study work establishes the principle that networks of neurons adapt to the presence of a toxic HIV protein and suggest that viewing EEG changes as an adaptive response might facilitate therapeutic intervention.
Categories
brain plasticity, dementia, healthinnovations, HIV, HIV-associated neurocognitive disorders, immunology, neurodegeneration, neuroinnovations
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